Abstract
Cytosine arabinoside (Ara-C) elicited a significant increase in the level of the enzyme glutamine synthetase (GS) while it markedly reduced overall RNA and protein synthesis in cultures of embryonic chick neural retina. This increase was analyzed by radioimmunochemical procedures and compared with the induction of GS by hydrocortisone (HC). Accumulation of GS in Ara-C-treated retinas was due to de novo synthesis of the enzyme; however, unlike the induction of GS by HC, Ara-C caused no measurable increase in the rate of GS synthesis. Ara-C facilitated GS accumulation largely by preventing degradation of the enzyme. Even though Ara-C inhibited the bulk of RNA synthesis in the retina, it did not stop the formation of GS-specific RNA templates. The progressive accumulation of these templates did not result in an increased rate of GS synthesis unless Ara-C was withdrawn from such cultures under suitable experimental conditions. The continuous presence of Ara-C imposed a reversible hindrance at the translational level which limited the rate of GS synthesis. The increase in retinal GS elicited by Ara-C was achieved through mechanisms which were quite different from those involved in HC-mediated induction of this enzyme.